Expression data from pre-iPSCs with a control, histone methyltransferase or Cbx3 (HP1g) knockdown
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE44084 | GEO | 2013/06/05
SECONDARY ACCESSION(S): PRJNA188521
REPOSITORIES: GEO
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Project description:Transition from a partially reprogrammed pre-iPSC state to iPSC state can be achieved by modulating levels of histone modifying enzymes or proteins that can bind to histone modifications We used microarrays to determine the gene expression profile of pre-iPSCs depleted for either 3 histone methyltransferases together or the HP1gamma protein pre-iPSCs were subjected to simultaneous siRNA mediated knockdown of Ehmt1, Ehmt2 and Setdb1- which is the 3XHMT sample that mediate H3k9me2/me3 or Cbx3( HP1gamma) or control siRNA to luciferase
2013-06-05 | E-GEOD-44084 | biostudies-arrayexpress
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Project description:Study of HP1 Knock Down on gene expression and splicing regulation in Human HeLa cells Maturation of pre-mRNAs is initiated co-transcriptionally. It is therefore conceivable that chromatin-borne information participates in alternative splicing. Here, we find that elevated levels of tri-methylation of histone H3 on lysine 9 (H3K9me3) are a characteristic of the alternative exons of several genes including CD44. On this gene, the chromodomain protein HP1gamma, frequently defined as a transcriptional repressor, facilitates inclusion of the alternative exons via a mechanism involving decreased RNA polymerase II elongation rate. In addition, accumulation of HP1gamma on the variant region of the CD44 gene stabilizes association of the pre-mRNA with the chromatin. Altogether, our data provide evidence for localized histone modifications impacting alternative splicing. They further implicate HP1gamma as a possible bridging molecule between the chromatin and the maturating mRNA, with a general impact on splicing decisions. Transcriptome analysis of siRNA anti-HP1gamma transfected HeLa cells on GeneChip® Human Exon 1.0 ST Arrays (Affymetrix). Control HeLa cells have been transfected with the same concentration of siRNA anti-GAPDH. Experiment has been done in experimental triplicates.
2011-02-27 | E-GEOD-25282 | biostudies-arrayexpress
Project description:Study of HP1 Knock Down on gene expression and splicing regulation in Human HeLa cells Maturation of pre-mRNAs is initiated co-transcriptionally. It is therefore conceivable that chromatin-borne information participates in alternative splicing. Here, we find that elevated levels of tri-methylation of histone H3 on lysine 9 (H3K9me3) are a characteristic of the alternative exons of several genes including CD44. On this gene, the chromodomain protein HP1gamma, frequently defined as a transcriptional repressor, facilitates inclusion of the alternative exons via a mechanism involving decreased RNA polymerase II elongation rate. In addition, accumulation of HP1gamma on the variant region of the CD44 gene stabilizes association of the pre-mRNA with the chromatin. Altogether, our data provide evidence for localized histone modifications impacting alternative splicing. They further implicate HP1gamma as a possible bridging molecule between the chromatin and the maturating mRNA, with a general impact on splicing decisions.
2011-02-27 | GSE25282 | GEO
Project description:We examined the locations of Cbx3 by chromatin immunoprecipitation in ESCs and pre-iPSCs Examination of Cbx3 in mESC (mouse embryonic stem cells) and pre-iPSCs (fibroblast derived partially reprogrammed cells)
2013-06-05 | E-GEOD-44242 | biostudies-arrayexpress
Project description:We examined the locations of Cbx3 by chromatin immunoprecipitation in ESCs and pre-iPSCs
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Project description:We report the application of Illumina Hi-Seq sequencing technology for high-throughput profiling of Cbx3/HP1g deposition in mammalian CD8+ effector T cells. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, genome-wide chromatin-state maps of mouse wt CD8+ effector T cells were generated. We find that Cbx3/HP1g negatively regulates the germinal center and high-affinity antibody responses in a CD8+ T-cell-dependent manner. CD8-restricted deletion of Cbx3/HP1g confers hightened effector and persistence capacity on CD8+ effector T cells. As a result, Cbx3/HP1g-deficient CD8+ effector T cells can efficiently control solid tumor growth in vairious mouse models (melanoma, ovarian and neuroblstoma).
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Project description:Induced pluripotent stem cell (iPSC) generation is similar to somatic cell nuclear transfer in oocytes, and this procedure can be used to generate ESCs, which suggests the contribution of oocyte-specific constituents. Here, we show that the mammalian oocyte-specific linker histone H1foo has beneficial effects on iPSC generation. Induction of H1foo with Oct4, Sox2, and Klf4 (OSKH) significantly enhanced the efficiency of iPSC generation. H1foo promoted in vitro differentiation characteristics with low heterogeneity in iPSCs. H1foo enhanced the generation of germline competent chimeric mice from iPSCs in a manner similar to that for ESCs. These findings indicate that H1foo contributes to the generation of higher-quality iPSCs. This experiment was designed to investigate the similarity of global gene transcriptome profile among OSKH iPSCs, OSK iPSCs and ESC.
2016-05-26 | GSE79515 | GEO
Project description:It has been suggested that the transcription factor Nanog is essential for the establishment of pluripotency during the derivation of embryonic stem (ES) cells and induced pluripotent stem (iPS) cells. However, successful reprogramming to pluripotency with a growing list of divergent transcription factors, at ever increasing efficiencies, suggests that there may be many distinct routes to a pluripotent state. Here, we have investigated whether Nanog is necessary for reprogramming murine fibroblasts under highly efficient conditions using the canonical reprogramming factors Oct4, Sox2, Klf4 and cMyc. In agreement with prior results, the efficiency of reprogramming Nanog-/- fibroblasts was significantly lower than that of control fibroblasts. However, in contrast to previous findings, we were able to reproducibly generate iPS cells from Nanog-/- fibroblasts that effectively contributed to chimeric mice. Thus while Nanog may be an important mediator of reprogramming it is not required for establishing pluripotency in the mouse, even under standard conditions. In order to further evaluate the equivalency of Nanog null iPSC to nanog null ESCs, we have performed RNAseq on two independent nanog null iPSC lines, as well as Nanog Null ESC, WT ESC and iPSCs as well as MEFs. As a negativve control for reprogramming we have analyzed a partially reprogrammed iPSC line. 2-4 biological replicates each of 7 conditions (WT MEFs, WT ESC, WT iPSC, WT partially reprogrammed iPSC (piPS), Nanog null ESC, Nanog null iPSC clone G2 and Nanog null iPSC clone G5)
2014-01-01 | E-GEOD-53212 | biostudies-arrayexpress
Project description:The methylation of histone 3 at lysine 9 (H3K9) is widely regarded as a major roadblock for cellular reprogramming and interference with associated methyltransferases such as EHMT1 and EHMT2 (also known as GLP and G9A) facilitates the derivation of induced pluripotent stem cells (iPSCs). In addition, activation of demethylases by ascorbic acid (AA) has become a common approach to facilitate the extensive epigenetic remodeling required for iPSC formation. The functional interaction between the H3K9 methylation machinery and AA-stimulated enzymes, and consequences of interfering with these pathways, remain insufficiently explored. Here, we show that reduction of EHMT1/2 activity paradoxically counteracts iPSC formation in an optimized reprogramming system in the presence of AA. At the cellular and molecular level, EHMT1/2 activity is required for efficient downregulation of somatic genes and transition into an epithelial state. Genetic interference with the demethylase KDM3B partially rescues the adverse effect of EHMT1/2 inhibition on iPSC formation. Transient inhibition of EHMT1/2 during reprogramming yields iPSCs that fail to efficiently give rise to viable mice, suggesting persistent molecular defects in these cells. Together, our observations document a more nuanced function of H3K9 methyltransferases during iPSC formation and suggest that the balancing of AA-stimulated enzymes by EHMT1/2 is required for efficient and error-free reprogramming to pluripotency.
2020-09-28 | GSE130490 | GEO